Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Ageing-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Department of Clinical Molecular Biology, University of Oslo, Oslo, Norway.
Curr Neuropharmacol. 2023;21(7):1477-1481. doi: 10.2174/1570159X20666220628153632.
Mitochondria are the main sites of energy production and a major source of metabolic stress. Not surprisingly, impairment of mitochondrial homeostasis is strongly associated with the development and progression of a broad spectrum of human pathologies, including neurodegenerative disorders. Mitophagy mediates the selective degradation of damaged organelles, thus promoting cellular viability and tissue integrity. Defective mitophagy triggers cellular senescence and prolonged neuroinflammation, leading eventually to cell death and brain homeostasis collapse. Here, we survey the intricate interplay between mitophagy and neuroinflammation, highlighting that mitophagy can be a focal point for therapeutic interventions to tackle neurodegeneration.
线粒体是能量产生的主要场所，也是代谢应激的主要来源。毫不奇怪，线粒体动态平衡的损害与广泛的人类病理学的发展和进展密切相关，包括神经退行性疾病。线粒体自噬介导受损细胞器的选择性降解，从而促进细胞活力和组织完整性。线粒体自噬缺陷会引发细胞衰老和长期神经炎症，最终导致细胞死亡和大脑内环境崩溃。在这里，我们调查了线粒体自噬和神经炎症之间的复杂相互作用，强调线粒体自噬可以成为治疗干预神经退行性变的焦点。
